
pmid: 15734682
Aging can be defined as progressive functional decline and increasing mortality over time. Here, we review evidence linking aging to nuclear DNA lesions: DNA damage accumulates with age, and DNA repair defects can cause phenotypes resembling premature aging. We discuss how cellular DNA damage responses may contribute to manifestations of aging. We review Sir2, a factor linking genomic stability, metabolism, and aging. We conclude with a general discussion of the role of mutant mice in aging research and avenues for future investigation.
DNA Repair, Biochemistry, Genetics and Molecular Biology(all), Longevity, Antigens, Nuclear, Genomic Instability, DNA-Binding Proteins, Mice, Animals, Sirtuins, Rad51 Recombinase, Tumor Suppressor Protein p53, Reactive Oxygen Species, Ku Autoantigen, Cellular Senescence, DNA Damage
DNA Repair, Biochemistry, Genetics and Molecular Biology(all), Longevity, Antigens, Nuclear, Genomic Instability, DNA-Binding Proteins, Mice, Animals, Sirtuins, Rad51 Recombinase, Tumor Suppressor Protein p53, Reactive Oxygen Species, Ku Autoantigen, Cellular Senescence, DNA Damage
| selected citations These citations are derived from selected sources. This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 836 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 0.1% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 1% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 0.1% |
